Basanti Biswal and U. C. Biswal
School of Life
Sciences, Sambalpur University, Jyoti Vihar 768 019, India
Leaf senescence although deteriorative
in nature, has been recognized as the last phase of the organs development, a highly
ordered process regulated by genes known as senescence associated genes (SAGs). Till now,
more than 30 SAGs have been isolated, cloned and characterized. The leaf when young and
mature, accumulates nutrients and exports them to growing parts of the plant during
senescence. The macromolecular degradation and their transport during senescence are
reported to be strictly controlled by genes. The genes are also reported to actively
participate in energy metabolism and supply metabolic energy for the transport of
nutrients. Through genetic regulation, the senescing leaves maintain cellular integrity
and potential not only for nutrient transport, but also for effective transcription and
translation of proteins. Although the genes specific for induction of senescence have not
yet been precisely identified, the down-regulation of photosynthetic genes has been
proposed to be the possible signal for up-regulation of SAGs and induction of senescence.
Leaf senescence is recognized as a process following a programmed cell death (PCD). The
regulatory elements of some of the SAGs are characterized and their response to senescence
inducing factors indicates scope for further studies on the molecular mechanism of signal
response coupling during foliar senescence.
A special section consisting of several articles on biology of aging appeared
in the 25 May 1998 issue of Current Science.
However, all these articles mostly describe data relating to biochemistry and molecular
biology of aging and senescence in animal systems only. Aging and senescence are used
interchangeably in case of animals but in plants, the process of senescence is better
defined as an active process and is well differentiated from aging which is considered to
be passive time-dependent degeneration. The basic molecular mechanism of senescence both
in plant and animal systems may be the same. The process involves expression of specific
Since senescence constitutes an internally regulated developmental process,
it has a logic in plant life and therefore, carries significant physiological
implications. A programmed senescence, is basically an adaptive mechanism and the death,
its consequence, therefore, takes place on the organisms own terms. In nature,
senescence in leaves is the best example that fits into this concept. Leaf senescence has
extensively been investigated in the last few years. The process, however, is not only
concerned with death but involves several events associated with massive mobilization of
nutrients in a highly ordered and regulated manner from senescing leaves to new leaves,
developing fruits, seeds and buds, thus contributing to the nutrient cycling. The
senescing leaves carry out these events and therefore remain viable and active. Although
there are limits for generalization and extrapolation of the mechanism of leaf senescence
in understanding the process in whole plants, the study however, provides vital clues to
the knowledge of basics of senescence as a process.
Senescence of a leaf is temporally regulated in a co-ordinated manner1,2.
The cellular components in the senescing leaves experience a sequential dismantling with a
perfect order3,4. Although the process operates under the active control of
genes, it is known to be modulated by environmental signals5. The precise
triggering mechanism of leaf senescence still remains unclear but it is proposed to be
induced by intrinsic and environmental factors5,6. In green leaves, the process
is mostly characterized by a loss in total chlorophyll7. In addition, the
degradation of macromolecules, namely proteins, nucleic acids, lipids and a decline in
photosynthesis, remobilization of nutrients and the dismantling of cellular organelles are
other major events associated with the process3,6. The genes regulating these
events are known as senescence associated genes (SAGs)5,8. More than 30 SAGs
are isolated, cloned and characterized in different plant systems.
This review describes the expression of the SAGs associated with
macromolecular degradation and mobilization of nutrients from senescing leaves. It also
describes the genes for maintaining the viability of senescing cells. The review very
briefly covers findings on chloroplast degradation during leaf senescence and
down-regulation of the photosynthetic genes as the possible factor for induction of leaf
senescence. Regulation of senescence-associated genes, with particular reference to study
of their promoters are also discussed. Some of the questions in this area, still
unanswered, are addressed in the concluding section.
Genes for macromolecular degradation
during leaf senescence
The turnover of macromolecules particularly proteins is a common occurrence
during plant growth and development. Although degradation of macromolecules is one of the
major events that occurs during leaf senescence, the process nevertheless involves the
synthesis of RNA and proteins de novo1,6.
Macromolecular degradation of senescing leaves is a pre-requisite for making transportable
nutrients that are subsequently remobilized to young and expanding organs of the plants.
Senescence-induced protein breakdown that has been well reported in many plant systems,
results in availability of transportable nitrogen6. The precise mechanism and
the type of specific proteases involved in protein breakdown, however, are yet to be known
but the possible participation of cysteine proteases and aspartic proteases in the process
has been suggested911.
The degradative enzymes may not be very specific to any developmental
sequence including senescence. For example, most of the enzymes that participate in the
degradation of macromolecules for reserve mobilization during germination also participate
in degradation during senescence1114. During tomato leaf senescence,
Drake et al.15 have isolated two cDNA
clones that exhibit homology with the genes for the cysteine proteinases. These genes for
synthesis of the proteases are also known to express during seed germination. Similarly,
the cDNA clones isolated from Arabidopsis
during senescence exhibit sequence identity with cysteine protease having a high degree of
homology with oryzain y and aleurain8, the proteases well known for their
action in the degradation of reserve proteins for the mobilization of nitrogen during seed
Smart et al.9 have
identified and characterized several genes associated with leaf senescence of maize
plants. Senescence shows enhanced expression of two genes, one exhibiting sequence
homology with cysteine proteases oryzain y from rice and the other with the
protein-processing enzyme of castor bean seeds. It is likely that these genes participate
in degradation of proteins and then mobilization of the breakdown products in
transportable form from senescing leaves to other parts of the plants. These observations
thus suggest that the genes for proteases for macromolecular degradation may not be
specific to senescence. In fact, a level of expression of the genes is also observed in
young and mature leaves, however, with their enhanced expression during senescence5.
In addition to the expression of genes for the proteases, senescence-induced enhanced
expression of genes for synthesis of nucleases18 and lipases19 for
degradation of nucleic acids and lipids, respectively, are also reported. The SAGs
relating to macromolecular degradation are not supposed to be associated with senescence
induction. The genes express only after initiation of the process9.
Participation of genes for export of
A leaf during its rapid development acts as a strong sink drawing nutrients
from other sources of the plant and is converted to a source of nutrients when it becomes
mature with full photosynthetic establishment. Maturity of the leaf is likely to send
signal(s) for a decline in photosynthesis, induction of senescence and subsequent
mobilization of resources to other growing regions. A functional shift from photosynthesis
to resource mobilization in senescing leaves significantly contributes to the optimization
of resource utilization by the whole plant. The leaf, at late stage of senescence with
rapid loss in photosynthetic activity and relatively high respiratory rate obviously
becomes obsolete and therefore, becomes a respiratory burden for plants. The plant,
therefore, rejects it by the process of abscission. Between the induction of senescence
and abscission, the resources accumulated in the leaf are mobilized to young and growing
parts. Various events associated with the mobilization process like degradation of
macromolecules, interconversion of metabolites to their transportable forms, and their
energy-dependent movement are tightly regulated. The remobilization of nutrients is a
complex, extensive but highly co-ordinated process involving up-regulation of several
genes (Figure 1). This is a mechanism that the plant has evolved to salvage the resources
it has already acquired before the obsolete senescing leaves are cast off.
The expression of specific genes has been reported to be associated with the
mobilization of breakdown products of the macromolecules during senescence. Different cDNA
clones homologous to the genes for proteases as described earlier6, like malate
synthatase13, glutamine synthatase20 and ribonuclease18
relating to macromolecular degradation and mobilization during senescence are isolated and
characterized (Figure 1).
Mobilization of nitrogen
Several enzymes participate in protein breakdown and subsequent transfer of
nitrogen. In addition to glutamate dehydrogenase, transaminase is known to be responsible
for shunting of nitrogen into glutamine and asparagine, the common mobile forms of
nitrogen6. The key enzyme responsible for the synthesis of glutamine is
glutamine synthatase (GS1). For recovery of nitrogen from senescing leaves, GS1 plays a
crucial role. The cDNA clones for GS1 have been isolated and their expression has been
examined in detail during senescence of radish cotyledons21. It is suggested
that the function of GS1 is
Figure 1. Up-regulation of several SAGs
(senescence associated genes) associated with the degradation of macromolecules and
transport of nutrients from senescing leaves. The transport involves metabolic energy,
namely ATP. The energy level is controlled by up-regulation of genes associated with
to convert ammonia to glutamine, a known transportable form of nitrogen that
is remobilized from senescing leaves to growing parts of plants. Structurally three cDNA
clones for the enzyme (GS1) have been characterized and two of them namely Gln 1:1 and Gln
1:3 have been shown to be expressed both during natural and dark-induced senescence as
revealed by Northern blot analysis21. A cDNA clone homologous to GS1 has been
shown to have enhanced expression during senescence in Brassica10. Its role has been attributed
possibly in the synthesis of glutamine and subsequently its transport (Figure 1).
Breakdown of lipids, its conversion
to sugars and their transport
The genes responsible for synthesis of the enzymes involved in
gluconeogenesis are reported to be significantly expressed during leaf senescence6.
A decline in photosynthesis during senescence may result in sugar starvation leading to
the activation of conversion of lipids to sugars (Figure 1). Thylakoid breakdown leads to
release of lipids, which are known to be converted to sugars through the glyoxylate cycle6,22,23.
The sugars produced by conversion of large amounts of lipids may be in excess than that
required for respiration of the senescing leaves and this may be exported to other growing
and demanding parts of the plant in transportable form. It appears that the expression of
genes for the enzymes participating in the process of gluconeogenesis for production of
sucrose plays an important role during senescence6,22 (Figure 1).
Mobilization of other nutrients
Leaf senescence also results in the breakdown of nucleic acids to purines and
pyrimidines, which ultimately degrade to small and transportable carbon and nitrogenous
compounds that are transported to growing parts of the plant6 (Figure 1).
In addition to mobilization of carbon and nitrogen, other nutrients like
sulphur and metallic ions are also known to be transported from senescing leaves. The
polypeptide of a cDNA clone that has sequence similarity with plant ATP sulphurylase has
been examined during senescence of Brassica10.
The enzyme ATP sulphurylase is known to participate in the biosynthetic pathway of
methionine and cysteine. During senescence, its enhanced expression may modulate the level
of cysteine and consequently its conversion to glutathione which plays a key role not only
in minimizing the level of toxic oxygen free radicals produced during senescence but may
also be involved in storage and transport of sulphur from senescing leaves to growing
parts of the plants.
Genes involved in maintenance of cell
integrity of senescing leaves
The progression of senescence involves energy and the process needs retention
of transcriptional potential for the expression of senescence-related genes. The leaves
also develop an efficient mechanism to minimize toxic levels of free radicals and maintain
a level of cell viability. Since the process is basically deteriorative in nature, the
senescing cells should have adaptational strategy to counter certain specific
deteriorative events in order to maintain respiratory metabolism, protect the cells
against the formation of free radicals and keep the trascription machinery active.
Senescence-induced increase in the level of expression of a cDNA clone having sequence
similarity with catalase gene, expression of the genes against pathogen attack and
up-regulation of the genes against metal toxicity support this proposition6.
The enhanced expression of genes for the synthesis of enzymes participating in the
respiratory process during senescence is discussed elsewhere in this review. Lipid
conversion to sugar is a major event favouring the proposition of energy maintenance of
senescing leaves6 (Figure 1).
Gene expression against infection
During leaf senescence of Brassica10,24
and Lycopersicon25, a significant
increase in the expression of homologues of pathogen-related (PR) genes has been observed.
The precise function of the products of PR genes during senescence still remains unclear.
However, PR proteins are known to protect the plants against pathogen attack and genes for
the proteins are therefore, known to be expressed during pathogen infection. Since
senescing leaves are relatively prone to pathogen attack, the PR protein may protect the
leaves against infection. On the other hand, some of the PR genes are also known to be
regulated by plant developmental factors. In addition to leaf senescence25,
reports are also available on expression of the genes in germinating and developing seeds26,27.
Supporting the proposition, Hanfrey et al.24
have shown genes similar to previously known PR genes expressed during early stages of
senescence of leaves not infected by any pathogen, suggesting a function of the genes not
necessarily related to pathogen infection. The genes might be playing a role in a
developmental signal transduction pathway associated with triggering of senescence in
addition to their role against infection.
Gene expression against free
Ferritins are iron-binding proteins that can store iron atoms and make them
available in soluble and metabolically useful forms. The metabolic significance of
senescence-induced increase in the expression of homologues of ferritin genes as reported
by Buchanan-Wollaston and Ainsworth10 in Brassica
may suggest that during senescence, the degradation of some of the cellular macromolecules
may result in release of free metals and consequently an increased pool of free iron. The
free iron is known to bring about a metal catalysed reaction6 for production of
oxygen-free radicals, leading to the damage of senescing cells. The possible role of
ferritin could be its participation in the formation of a complex with iron and transport
of iron from senescing leaves to growing parts of the plant6. In a similar way,
the significance of an enhanced expression of homologues of metallothionin genes as
reported in Arabidopsis28 and Brassica10 could be explained. During
senescence, metallothionin may bind with free metal ions released from protein breakdown
and thus make them available for storage and transport. In the process, the production of
free radicals catalysed by the free metal ions is minimized. In spite of these
adaptational mechanisms, the senescing leaves also develop other kinds of strategy to
minimize the level of free radicals including toxic oxygen radicals, which are
significantly increased due to many factors including a loss in the activity of superoxide
dismutase29. Senescence-induced enhanced expression of the catalase gene as
reported by Thomas and de Villiers28 and Buchanan-Wollaston and Ainsworth10
may help in reducing the pool of these radicals.
Degradation of the chloroplast, its
significance and its possible role in initiation of leaf
Chloroplast in a green leaf is the earliest and major target of
senescence-induced catabolism3,4. Changes in the structural organization and
function of chloroplasts have been extensively investigated during the process in many
laboratories in various plant systems1,2. The organelle exhibits both
quantitative and qualitative changes in the pigments29,30, macromolecules3,31,
molecular structure32,33, thylakoid organization34 and in the
enzymes that participate in carbon dioxide fixation in stroma7,35,36. The
disassembly of thylakoid membranes includes unstacking of grana followed by breakdown of
membranes to plastoglobuli in addition to loss in primary photochemical reactions and
breakdown of Rubisco, a major protein of green leaves37.
The proteases responsible for degradation of organelle-located proteins are
yet to be characterized in detail, although several endopeptidases in chloroplasts have
been reported by several authors1,38,39. It is possible that the initial steps
for cleavage of these proteins occur in the organelle itself. Further, the presence of
proteases in chloroplasts, degradation of proteins in the isolated organelle40,41
and the report on degradation of SSU of Rubisco in the chloroplast by a proteolytic system
encoded by a nuclear gene42 may indicate action of the organelle protease in
degradation of its protein. This is further supported by the observation of ClpP and ClpC
protease subunits in chloroplasts of Arabidopsis39.
The expression of chloroplast gene with sequence homology to the catalytic subunit of
ATP-dependent bacterial protease ClpP has been observed. Secondly, leaf senescence is
reported to induce expression of early responsive dehydration gene (erd1) encoding a protein with similarity to
regulatory ATPase subunit (ClpA) of Clp protease43. ClpA interacts with ClpP
synthesized in chloroplasts and brings about the degradation of proteins during leaf
senescence43. However, the proteolytic degradation of chloroplasts during
senescence has to be considered in the background of participation of vacuolar protease.
Reports are available on the degradation of pigments and proteins of chloroplasts by
The question being presently addressed is what really initiates dismantling
of chloroplast during senescence? Experimental evidences may suggest the degradation to be
initiated by nuclear genes. A delay in senescence in nuclear gene mutants, retardation of
the process by nuclear specific RNA and protein synthesis inhibitors and retardation of
chlorophyll loss in isolated chloroplasts or anucleate cells1,2 support this
proposition. On the other hand, the non-nuclear gene responsible for senescence has been
reported to reside in the chloroplast itself45. It appears that we may have to
wait for the answer.
Significance of chloroplast degradation
induction of leaf senescence
Chloroplast catabolism plays a key role in the resource mobilization in
plants. During senescence, it is the major source of carbon and nitrogen ultimately
released during seed formation. About 90% of nitrogen exported from the organelle are
Rubisco in stroma and light harvesting chlorophyll-binding proteins in thylakoid membrane46.
The genes for these proteins and other photosynthesis-associated genes (PAGs) are known to
be up-regulated during leaf development and expansion. However, during transition in the
functional behaviour of the leaf when it switches over from a photosynthetic organelle to
a storage organelle for transport, these genes are down-regulated5,8,25,4751.
The expression of two photosynthetic genes for Rubisco small subunit (rbcs) and Chla/b-binding
protein (cab) were extensively examined by Hensel et
al.8 during leaf senescence of Arabidopsis
along with two marker genes associated with senescence that are up-regulated. These
authors proposed a model suggesting the possibility of a down-regulation of photosynthetic
genes as a cause for induction of leaf senescence and up-regulation of the genes for
macromolecular degradation and their subsequent transport. A decline in photosynthesis
intrinsically by a developmental signal or by various biotic and abiotic stress factors
may initiate the senescence process as shown in Figure 2.
Although it is difficult to quantitatively find the threshold of
photosynthetic decline that triggers foliar senescence, the compensation point when the
leaf loses its potential to contribute the fixed carbon to other parts of the plant body,
could initiate the process of senescence52.
Molecular mechanism of foliar
Leaf senescence as a programmed cell
Recently, attempts were made to extrapolate the molecular mechanism of
programmed cell death (PCD) of ani-
Figure 2. Initiation of leaf senescence
by down-regulation of photosynthetic genes. A decline in photosynthesis by biotic/abiotic
stress factors may directly or indirectly through modulating the developmental signal,
cause induction of senescence. (Numbers in brackets indicate references).
mals in understanding the molecular events associated with senescence and
cell death in plants51,52. Apoptosis in certain vertebrate tissues as
characterized by diagnostic features of PCD like activation of endonuclease
and cellular shrinkage is comparable with shrinkage of the cytoplasm and nucleus with
fragmentation of DNA leading to cell death induced by low cell density in carrot cell
suspension53. Similarly, the formation of tracheary elements of xylem has been
used as a plant model of PCD54. When tracheary elements mature, they lose their
nuclei, cell contents and form a hollow tube with secondary cell wall thickening. These
events involve participation of genes suggesting occurrence of PCD54. The PCD
during the xylogenesis with loss of nuclei, however, may be different from the programmed
senescence of many other tissues where the nuclei largely remain unaltered during
The organized physiological, biochemical and genetic events exhibited by the
developmentally-mediated senescence in leaves leading ultimately to death, imply that the
process is programmed. The expression of specific genes and synthesis of cascade of
proteins during induction and progress of the process may clearly recognize leaf
senescence as a type of PCD, which appears to share many common points with PCD in animals52.
On the other hand, apoptosis, a specific category of PCD might have a different logic in
plants. During senescence, the disappearance of chloroplast DNA, the central
characteristic of apoptosis has been observed in plants52. However, it is not
clear whether the loss of DNA is really apoptic in nature or it has a physiological
significance in the background of mobilization of phosphorus, a breakdown product of the
nucleic acid from senescing leaves to other growing parts of the plants. However, a clear
understanding of the PCD path during leaf senescence and its significance in plant life
need further investigation.
Signals for expression of
The possible operation of signals from developing sink, hormone signals and
changes in the level of metabolites regulating expression of senescence-associated genes
have been suggested6. However, studies on signal perception, processing and
expression of genes for initiation of senescence in leaf cells leading to death are meagre6.
A reduction in the level of cytokinins, a possible hormonal signal may lead to
induction/enhancement of foliar senescence which has been shown to be significantly
retarded by its exogenous application or its overproduction in transgenic plants51.
Similarly, the metabolism of ethylene during fruit ripening has been extensively examined6,51.
The hormone is known as a signalling molecule for fruit ripening and its inhibition
by antisense technology leads to retardation of ripening. The possibility of ethylene as a
signalling molecule regulating foliar senescence has also been suggested6,51,
which may indicate a common signal transduction pathway of PCD both during senescence and
fruit ripening. The other type of signalling system, extensively examined for induction of
foliar senescence, is associated with the development of reproductive structures in
plants. The onset of reproduction may produce a senescence-related signal that is
transported to leaves for senescence induction55. Jasmonic acid has been
suggested as a possible candidate, which of course needs confirmation with strong
experimental support6. Recently, an attempt was made to characterize signalling
mechanisms in a relatively simple system, namely single cell suspension of carrot cells,
where PCD pathway is induced by low cell density53. The authors suggest that
plants can regulate PCD as in the case of animals by a kind of social signalling system.
The possibility of involvement of Ca2+ and protein phosphorylation in this
signal transduction pathway has been discussed.
All these signalling systems, in addition to the down-regulation of
photosynthesis as a possible signal for induction of senescence-related genes as discussed
in previous section, are discussed in different plant systems in different experimental
conditions. It is, therefore difficult to generalize the data in this area for emergence
of an integrated picture of signalling system. It is, however, possible that these
signalling systems with different pathways may meet at a common point leading to
down-regulation of photosynthetic genes that trigger foliar senescence.
Regulation of gene action
The induction of leaf senescence is suggested to be associated with down-
and/or up-regulation of several genes8. A few marker genes specifically
expressed during senescence are also reported6,8,12. The question is, what does
really control the switching on or off of these genes? Although a little is known about
the precise changes that lead to the expression and/or suppression of SAGs accompanying
senescence, recent experiments and analysis of promoters of some of the SAGs reveal cis-acting elements of the promoter sensitive to
senescence-inducing agents. Chung et al.56
have worked on the activity of the promoter of a senescence-associated gene (sen1) of Arabidopsis.
The promoter of the gene was well characterized. It was fused with GUS, a reporter gene
and then introduced to tobacco plants to investigate the activity of the promoter to
senescence-inducing factors like darkness, variation in the sugar level and ABA
treatments. The promoter activity was assessed by measuring the GUS gene product.
Darkness, exogenous addition of ABA and sugar starvation induced by DCMU treatment are
shown to significantly promote GUS expression, suggesting that these senescence-inducing
agents might be operating through signalling systems to regulate gene expression through
On the other hand, the genetic regulation of retarding action of leaf
senescence by cytokinins has been examined. Gan and Amasino51 have used the
promoter of a senescence-specific gene for expression of IPT, the enzyme catalysing the
first controlling step of cytokinin biosynthesis. The novelty of their work is that the
activity of the promoter depends on the onset of senescence in leaves. The promoter,
therefore, activates production of cytokinins only when leaves start experiencing
senescence. Production of the hormone prevents furthering of the process, which brings
about attenuation of the promoter and thus prevents an excess accumulation of the hormone.
Further work in this area may provide clues about the nature of cis-acting elements of senescence-associated genes
and their interaction with transacting factors and thus reveal the story of signal
response coupling during senescence.
Conclusions and perspectives
The study of leaf senescence at the molecular level is rather recent. In
spite of the significant progress made in plant molecular biology, several questions
remain unanswered in understanding the process, some of which are addressed here:
(i) Many cDNA
clones relating to leaf senescence are isolated and the clones are identified on the basis
of sequence homology with the proteins and nucleic acids in the database search. Although
their functions are extrapolated with known functions of the genes, the implications of
the function in understanding the mechanism of induction and progress of senescence still
remains unclear. Secondly, we have failed to identify some of the cDNA clones very
specific to senescence process because of lack of sequence homology of these clones. With
advancement in plant molecular genetics, particularly in the area of sense and antisense
transformation of plants, we should be able to have further insight into the nature of
gene products and their metabolism that may help in understanding the mechanism of
the genes associated with leaf senescence are isolated and characterized, the precise
nature of the regulation of their expression is not clearly understood. The analysis of
promoters of many senescence-related genes reveal no uniformity in sequence elements,
which would suggest that regulation of these genes during the process is complex and is
controlled by several factors through different signal transduction pathways. Some
progress has been made in isolation and characterization of the promoters of a few SAGs.
But identification of the transacting factors and their interaction with promoter
sequences for regulation of the process are not successfully investigated yet.
(iii) Not much is
known about the nature of the signals and their transduction in induction of leaf
senescence. Because of the complex nature of genetic regulation of the process, it is not
yet possible to identify the signal transduction pathways between the perception of
specific signals and initiation of cascades of gene expression and finally the phenotypic
expression of the senescence syndrome. Secondly, information on the nature of initial
signals and their transduction, whether the same or different in induced and natural
senescence are not available. The nature of signals in the senescence process induced by
the environmental stress may be different from that of the natural age-dependent process.
In monocarpic plants, the initiation of leaf senescence and development of reproductive
organs appear to involve a tight correlation possibly controlled by a co-ordinated
signalling system. However, the precise nature of biochemical routes of signal processing
is not unequivocally established.
is one of the major targets of senescence-induced degradation. In fact, a major amount of
nitrogen to be exported from senescing leaves comes from the organelle. However, the
mechanism of protein degradation in chloroplast and identification of proteases
responsible for degradation of the macromolecules are yet to be known.
(v) A good
plant model for the study of leaf senescence is still lacking. The cells in a single leaf
never get senescent uniformly and simultaneously. Although dark-induced senescence and
senescence of excised leaves provide a good model so far as cell synchrony is concerned,
these models have their own limitations. The problem of choosing a better system for the
study of molecular biology of leaf senescence still remains unsolved.
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